Internal Medicine
1 questionsIn which condition is the Doll's Eye Reflex tested?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 171: In which condition is the Doll's Eye Reflex tested?
- A. Hemiplegic
- B. Paraplegic
- C. Cerebral palsy
- D. Unconscious patients (Correct Answer)
Explanation: ***Unconscious patients*** - The **Doll's Eye Reflex**, also known as the **oculocephalic reflex**, is a brainstem reflex used to assess brainstem function in **comatose or unconscious patients** [1]. - It is positive if the eyes move in the opposite direction to the head turn, indicating intact brainstem pathways [1]. *Hemiplegic* - **Hemiplegia** refers to paralysis on one side of the body, often due to stroke or brain injury. - While it can be associated with altered consciousness, the Doll's Eye Reflex specifically tests brainstem integrity in unconscious states, not the motor deficits of hemiplegia itself. *Paraplegic* - **Paraplegia** is paralysis affecting the lower half of the body. - This condition primarily involves spinal cord damage and does not directly relate to the assessment of brainstem function using the Doll's Eye Reflex. *Cerebral palsy* - **Cerebral palsy** is a group of disorders affecting movement, muscle tone, or posture, caused by damage to the developing brain. - While individuals with cerebral palsy may have neurological impairments, the Doll's Eye Reflex is not a primary diagnostic or assessment tool for this chronic condition; it is used acutely in unconscious states.
Pathology
4 questionsWhat is the characteristic feature of neuropraxia?
Which of the following is not considered an example of excess tissue growth?
Which of the following is not an apoptotic gene?
Which substance plays a significant role in the tumor metastasis cascade?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 171: What is the characteristic feature of neuropraxia?
- A. Damage to the endoneurium
- B. Damage to the epineurium
- C. No structural damage to the nerve (Correct Answer)
- D. Damage to the axon
Explanation: ***No structural damage to the nerve*** - **Neuropraxia** is the mildest form of nerve injury, characterized by a **temporary block in nerve conduction** without structural damage to the axon or surrounding connective tissues. - This typically results in **temporary sensory and/or motor deficits** that fully resolve within weeks to months. *Damage to the endoneurium* - Damage to the **endoneurium** would indicate a more severe injury, such as **axonotmesis**, where the axon is damaged but the connective tissue sheaths are preserved. - This level of injury suggests that wallerian degeneration would occur distal to the lesion, leading to **slower and incomplete recovery**. *Damage to the epineurium* - Damage to the **epineurium**, along with the endoneurium and perineurium, signifies **neurotmesis**, the most severe nerve injury. - This involves a **complete transection of the nerve**, requiring surgical intervention for any chance of functional recovery. *Damage to the axon* - Damage to the **axon** itself, often alongside preserved connective tissues, is characteristic of **axonotmesis**. - While recovery is possible through axonal regeneration, it is **slower and less complete** than in neuropraxia.
Question 172: Which of the following is not considered an example of excess tissue growth?
- A. Granulation tissue (Correct Answer)
- B. Neoplasia
- C. Hyperplasia
- D. Fibrosis
Explanation: ***Granulation tissue*** - Granulation tissue is a normal part of the healing process and does not represent an **excessive growth** of tissue [3]. - It consists mainly of **new connective tissue** and blood vessels formed during healing, rather than a pathological proliferation [3]. *Hyperplasia* - Hyperplasia is characterized by an **increase in the number** of cells in a tissue, leading to tissue enlargement [1][2]. - This process is often a response to a stimulus, such as hormonal changes or injury, indicating **excess tissue growth** [2]. *Neoplasia* - Neoplasia refers to the **abnormal proliferation** of cells, forming a neoplasm or tumor, which can be benign or malignant. - This is a clear example of **excess tissue growth**, as it involves uncontrolled cell division. *Fibrosis* - Fibrosis implies the formation of excess **fibrous connective tissue**, leading to a stiff or thickened tissue, signifying abnormal tissue growth [4]. - It often results from chronic inflammation or injury, again reflecting **excessive tissue** formation [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 87-88. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 85-87. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 105-106. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 111-112.
Question 173: Which of the following is not an apoptotic gene?
- A. Mcl-1
- B. Bax
- C. P53
- D. n-myc (oncogene) (Correct Answer)
Explanation: ***n-myc*** - **n-myc** is primarily known for its role in **cell proliferation and differentiation**, not specifically associated with apoptosis [2]. - It is an **oncogene** that can contribute to tumorigenesis, but does not directly regulate apoptotic pathways [3]. *P53* - **P53** is a well-known **tumor suppressor gene** that plays a crucial role in inducing apoptosis in response to DNA damage [1]. - Activation of P53 leads to the transcription of genes that promote cell death, thus it is definitely an apoptotic gene [1]. *Bax* - **Bax** is a pro-apoptotic member of the **Bcl-2 family**, promoting apoptosis by facilitating mitochondrial outer membrane permeabilization [4,5]. - It plays a direct role in the apoptotic pathway, making it an important apoptotic gene [5]. *Mcl-1* - **Mcl-1** is an anti-apoptotic member of the **Bcl-2 family**, which helps prevent apoptosis by inhibiting pro-apoptotic factors [2,3]. - Its function is to **promote cell survival**, not apoptosis, but it is still classified as part of the apoptotic regulatory network [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 65-67. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 80-81.
Question 174: Which substance plays a significant role in the tumor metastasis cascade?
- A. TNF-alpha
- B. CD99
- C. NM23
- D. MMP-2 (Matrix Metalloproteinase-2) (Correct Answer)
Explanation: ***Collagenase IV*** - Collagenase IV is involved in the **degradation of extracellular matrix**, facilitating tumor invasion and metastasis [1,2]. - It plays a crucial role in breaking down **type IV collagen**, a major component of the **basement membrane**, allowing cancer cells to migrate [2]. *TNF-alpha* - While TNF-alpha is a cytokine that can promote **tumor growth**, it is not directly involved in the **metastatic cascade** like collagenase IV [3,4]. - It primarily functions in **inflammation** and immune response, affecting tumor microenvironment rather than directly facilitating invasion. *NM23* - NM23 is noted for its potential role as a **tumor suppressor**, and lower levels are associated with metastasis. - However, it does not play a direct role in the *metastatic cascade* itself [3,4], as it primarily influences **tumor progression** rather than matrix degradation. *CD99* - CD99 is a cell adhesion molecule implicated in **cell migration**, but it is not a significant factor in the **enzymatic breakdown** of tissue during metastasis [1,2]. - Its expression has more to do with **cell adhesion characteristics**, rather than directly promoting invasive capabilities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 315-316. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 232-233. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 314-315. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 233-234.
Physiology
5 questionsWhich of the following statements is TRUE regarding the Bohr effect?
What is the Haldane Effect?
What is the total surface area of the respiratory membrane in a healthy adult human?
Which part of the sympathetic nervous system is responsible for secreting catecholamines?
What is one of the specific functions of the primary motor cortex located on the anterior edge of the pre-central gyrus?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 171: Which of the following statements is TRUE regarding the Bohr effect?
- A. Decreased affinity of Hb to O2 is associated with increased pH & decreased CO2
- B. Decreased affinity of Hb to O2 is associated with increased pH & CO2
- C. Decreased affinity of Hb to O2 is associated with decreased pH & increased CO2 (Correct Answer)
- D. Decreased affinity of Hb to O2 is associated with decreased pH & decreased CO2
Explanation: ***Decreased affinity of Hb to O2 is associated with decreased pH & increased CO2*** - The **Bohr effect** describes how **hemoglobin's (Hb) affinity for oxygen (O2) decreases** in the presence of increased **acidity (decreased pH)** and higher **carbon dioxide (CO2)** concentrations. - This physiological adaptation ensures that O2 is **released more readily** to tissues that are actively metabolizing (e.g., muscle during exercise), as these tissues produce more CO2 and lactic acid, leading to a drop in pH. *Decreased affinity of Hb to O2 is associated with increased pH & decreased CO2* - An **increased pH** (more alkaline) and **decreased CO2** actually **increase Hb's affinity for O2**, shifting the oxygen dissociation curve to the left. - This scenario promotes **oxygen loading** onto hemoglobin, typically occurring in the lungs rather than O2 release in the tissues. *Decreased affinity of Hb to O2 is associated with increased pH & CO2* - This statement combines an **increased pH** (which increases Hb-O2 affinity) with **increased CO2** (which decreases Hb-O2 affinity), leading to a contradictory and incorrect physiological effect based on the Bohr principle. - The net effect of an increased pH would typically dominate in terms of O2 binding. *Decreased affinity of Hb to O2 is associated with decreased pH & decreased CO2* - While **decreased pH** does reduce Hb's affinity for O2, **decreased CO2** would tend to increase it. - Therefore, this combination does not accurately represent the primary conditions that lead to a significant decrease in Hb-O2 affinity as described by the Bohr effect in active tissues.
Question 172: What is the Haldane Effect?
- A. O2 delivery by increased CO2
- B. CO2 delivery by increased CO2
- C. CO2 delivery by increased O2 (Correct Answer)
- D. O2 delivery by increased CO
Explanation: ***CO2 delivery by increased O2*** - The **Haldane effect** describes how **oxygenation of hemoglobin** decreases its affinity for **carbon dioxide (CO2)**, leading to the release of CO2 from the blood. - This is crucial in the lungs, where high oxygen levels promote CO2 unloading for exhalation. *O2 delivery by increased CO2* - This describes the **Bohr effect**, where an increase in **carbon dioxide (CO2)** or acidity in the tissues causes hemoglobin to release **oxygen (O2)**. - The Haldane effect is the converse, relating oxygen binding to CO2 release, not the other way around. *CO2 delivery by increased CO2* - This statement is inherently circular and does not describe a physiological effect. - It confuses the mechanism with the substance being transported. *O2 delivery by increased CO* - **Carbon monoxide (CO)** has a much higher affinity for hemoglobin than oxygen, forming **carboxyhemoglobin** and impairing oxygen delivery. - This is related to **carbon monoxide poisoning**, not a physiological regulatory effect like the Haldane or Bohr effects.
Question 173: What is the total surface area of the respiratory membrane in a healthy adult human?
- A. 30 m2
- B. 50 m2
- C. 75 m2 (Correct Answer)
- D. 100 m2
Explanation: ***75 m²*** - The **total surface area** of the respiratory membrane in a healthy adult human is approximately **70-80 m²**, with 75 m² being the most accurate estimate among the given options. - This large surface area is primarily attributed to the presence of approximately **300-500 million alveoli**, which are crucial for efficient gas exchange. - Modern measurements using **stereological techniques** have refined earlier estimates and established this range as the current standard. *100 m²* - This value represents an **older estimate** that has been revised downward with more accurate measurement techniques. - While historically cited in older textbooks, current physiological data supports a **smaller surface area** of approximately 70-80 m². *30 m²* - This value is significantly **underestimated** for the total respiratory membrane surface area. - Such a small surface area would result in highly **inefficient gas exchange**, leading to severe respiratory compromise and inability to meet metabolic demands. *50 m²* - While larger than 30 m², this is still an **underestimation** of the full respiratory membrane surface area. - It does not adequately account for the extensive and intricate branching of the **respiratory bronchioles** and the vast number of alveolar sacs.
Question 174: Which part of the sympathetic nervous system is responsible for secreting catecholamines?
- A. Cardiac ganglion
- B. Cervical sympathetic chain
- C. Adrenal medulla (Correct Answer)
- D. Thoracic sympathetic chain
Explanation: ***Adrenal medulla*** - The adrenal medulla acts as a modified **sympathetic ganglion**, directly innervated by **preganglionic sympathetic fibers**. - Upon stimulation, it releases a high concentration of **epinephrine** (adrenaline) and a smaller amount of **norepinephrine** (noradrenaline) into the bloodstream, acting as hormones. *Cardiac ganglion* - **Cardiac ganglia** are parasympathetic ganglia located in the heart, involved in regulating heart rate and contractility via acetylcholine release. - They do not secrete **catecholamines** but rather act as relay stations for parasympathetic innervation. *Cervical sympathetic chain* - The **cervical sympathetic chain** primarily innervates structures in the head, neck, and upper limbs, influencing functions like pupils, salivary glands, and sweat glands. - While it contains sympathetic neurons, its primary role is not the systemic release of **catecholamines** into the bloodstream. *Thoracic sympathetic chain* - The **thoracic sympathetic chain** provides sympathetic innervation to organs in the thoracic and abdominal cavities, influencing heart rate, bronchodilation, and visceral blood flow. - Like other sympathetic ganglia, it releases norepinephrine at target organ synapses, but it does not serve as a major endocrine gland for systemic catecholamine release.
Question 175: What is one of the specific functions of the primary motor cortex located on the anterior edge of the pre-central gyrus?
- A. Control of voluntary movement (Correct Answer)
- B. Increase extensor muscle tone
- C. Perception of pain
- D. Inhibition of stretch reflex
Explanation: ***Control of voluntary movement*** - The **primary motor cortex (M1)**, located in the **precentral gyrus**, is critically involved in generating neural impulses that control the execution of **voluntary movements**. - It plays a key role in **planning and executing complex, skilled movements**, especially of the distal musculature. *Increase extensor muscle tone* - While motor pathways influence muscle tone, the primary motor cortex's most specific role is not simply increasing extensor tone; rather, it coordinates a wide range of movements involving both flexors and extensors. - **Spasticity** or increased muscle tone (often extensor) is more commonly associated with damage to the **corticospinal tracts (upper motor neuron lesions)**, which *prevents* the fine-tuning inhibitory control from the cortex. *Perception of pain* - **Pain perception** is primarily processed in the **somatosensory cortex** (postcentral gyrus), limbic system, and insula, not the primary motor cortex. - The primary motor cortex is responsible for **motor output**, not sensory interpretation. *Inhibition of stretch reflex* - While descending motor pathways can modulate spinal reflexes, the direct and primary function of the primary motor cortex is not the specific inhibition of the stretch reflex. - The **gamma motor system** and other spinal interneurons are more directly involved in modulating the sensitivity of the stretch reflex.